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Pulmonary gas transport has not been typically recognized as a limiting factor to physical
exercise. Dempsey et al. (1984; 1986) have suggested that the pulmonary system remains
unchanged despite chronic aerobic training. Adaptations to other physiological systems may
impose metabolic demands which the respiratory system can not meet. In essence, the lung's
capacity for gas exchange becomes surpassed by other training adaptations. Supporting evidence
is seen as decreases in arterial oxygenation at near maximal work rates in highly trained male
endurance athletes (Dempsey et al., 1984; Powers et al., 1988; 1989; Hopkins and McKenzie
1989). Decreased arterial oxygenation has been termed exercise-induced arterial hypoxemia (EIH),
and has direct consequences on VO₂max (Lawler et al., 1988; Powers et al., 1989; Martin and
O'Kroy, 1993) and maximal performance capacity (Koskolou and McKenzie, 1994). It is
estimated that approximately fifty percent of highly trained male endurance athletes exhibit EIH
(Powers et al., 1988; 1993; Martin et al., 1992b). One mechanism that has been advanced to
explain this phenomenon is a diffusion limitation. Diffusion capacity of the lung (DL) may be
depressed during exercise and not allow for complete gas equilibrium to occur. If a structural
alteration were present during exercise, it would continue to depress DL during recovery.
To investigate the time course of change in pulmonary diffusion capacity for carbon
monoxide (DL[sub co]) ten (N=10) highly trained male cyclists (HT) and ten (N=10) moderately (MT)
male subjects were selected for this study. Subjects cycled to exhaustion to determine maximal
oxygen consumption (VO₂max) on an electronically braked cycle ergometer (Mijnhardt KEM-3)
(mean ± SD; HT VO₂max = 68.0 ± 4.9; MT VO₂max = 51.6 ± 4.7 mL-kg⁻¹Emin⁻¹). Percent
arterial oxygen saturation (%SaO₂) was monitored by a pulse oximeter (Ohmeda Biox 3740) to
determine if subjects demonstrated exercise-induced arterial hypoxemia (defined as %SaO₂ ≤ 91%)
(%SaO₂min HT = 91.4 ± 1.6; MT = 94.6 ± 1.1). At a second data collection period, pulmonary
function testing was performed. All subjects demonstrated normal pulmonary function. Initial
diffusion measurements were made to obtain resting DL[sub CO]. diffusion capacity of the alveolar
membrane (DM), and pulmonary capillary blood volume (Vc). Both spirometry and diffusion measurements were made using the same apparatus (Collins PLUS DS II). DM and Vc were
calculated by measuring DL[sub CO] at two inspired O₂ concentrations using the technique of Roughton
& Forster (1957). Subjects then cycled to fatigue at a workrate that corresponded to the highest
workrate attained during the VO₂max test. Expired gases and %SaO₂ data were collected during
the time to fatigue cycle test. Five additional measurements of pulmonary diffusion were made at
1, 2, 4, 6 and 24 hours following the cycle test.
One hour post-exercise, DL[sub CO] was significantly decreased in both groups compared to
baseline. The decrease reached a minimum value at 6 hrs and approached normal values 24 hrs
after the exercise. Only HT subjects exhibited EIH yet both groups experienced similar changes in
DL[sub CO] The correlation between %SaO₂min and change in DL[sub CO] was low (r=-0.3), implying that
EIH can not be explained by post exercise decrease in DL[sub CO]. The change in DL[sub CO] can be
explained primarily by a parallel decrease in Vc. Vc decreased below baseline values in both
groups, perhaps indicating a compensatory shunting mechanism. A smaller degree of change was
observed in DM, and played less of a role in the decreased DL[sub CO]-
The results of this study are the first to compare diffusion capacity in two separate groups,
based on training status, following maximal exercise. Both moderately trained and highly trained
subjects exhibited similar decreases in pulmonary diffusing capacity. This supports the theory that
the lung may not adapt to aerobic training and behaves in a similar manner regardless of training
status.

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